20
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Pre-exposure to Lower-Level Noise Mitigates Cochlear Synaptic Loss Induced by High-Level Noise

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The auditory sensory organs appear to be less damaged by exposure to high-level noise that is presented after exposure to non-traumatizing low-level noise. This phenomenon is known as the toughening or conditioning effect. Functionally, it is manifested by a reduced threshold shift, and morphologically by a reduced hair cell loss. However, it remains unclear whether prior exposure to toughening noise can mitigate the synaptic loss induced by exposure to damaging noise. Since the cochlear afferent synapse between the inner hair cells and primary auditory neurons has been identified as a novel site involved in noise-induced cochlear damage, we were interested in assessing whether this synapse can be toughened. In the present study, the synaptic loss was induced by a damaging noise exposure (106 dB SPL) and compared across Guinea pigs who had and had not been previously exposed to a toughening noise (85 dB SPL). Results revealed that the toughening noise heavily reduced the synaptic loss observed 1 day after exposure to the damaging noise. Although it was significant, the protective effect of the toughening noise on permanent synaptic loss was much smaller. Compared with cases in the control group without noise exposure, coding deficits were seen in both toughened groups, as reflected in the compound action potential (CAP) by signals with amplitude modulation. In general, the pre-exposure to the toughening noise resulted in a significantly reduced synaptic loss by the high-level noise. However, this morphological protection was not accompanied by a robust functional benefit.

          Related collections

          Most cited references88

          • Record: found
          • Abstract: found
          • Article: not found

          The role of oxidative stress in noise-induced hearing loss.

          Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and with these new insights comes hope for possible prevention or treatment. Underlying the classic set of cochlear pathologies that occur as a result of noise exposure are increased levels of reactive oxygen species (ROS) that play a significant role in noise-induced hair cell death. Both necrotic and apoptotic cell death have been identified in the cochlea. Included in the current review is a brief review of ROS, along with a description of sources of cochlear ROS generation and how ROS can damage cochlear tissue. The pathways of necrotic and apoptotic cell death are also reviewed. Interventions are discussed that target the prevention of noise-induced hair cell death: the use of antioxidants to scavenge and eliminate the damaging ROS, pharmacological interventions to limit the damage resulting from ROS, and new techniques aimed at interrupting the apoptotic biochemical cascade that results in the death of irreplaceable hair cells.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates.

            Acoustic overexposure can cause a permanent loss of auditory nerve fibers without destroying cochlear sensory cells, despite complete recovery of cochlear thresholds (Kujawa and Liberman 2009), as measured by gross neural potentials such as the auditory brainstem response (ABR). To address this nominal paradox, we recorded responses from single auditory nerve fibers in guinea pigs exposed to this type of neuropathic noise (4- to 8-kHz octave band at 106 dB SPL for 2 h). Two weeks postexposure, ABR thresholds had recovered to normal, while suprathreshold ABR amplitudes were reduced. Both thresholds and amplitudes of distortion-product otoacoustic emissions fully recovered, suggesting recovery of hair cell function. Loss of up to 30% of auditory-nerve synapses on inner hair cells was confirmed by confocal analysis of the cochlear sensory epithelium immunostained for pre- and postsynaptic markers. In single fiber recordings, at 2 wk postexposure, frequency tuning, dynamic range, postonset adaptation, first-spike latency and its variance, and other basic properties of auditory nerve response were all completely normal in the remaining fibers. The only physiological abnormality was a change in population statistics suggesting a selective loss of fibers with low- and medium-spontaneous rates. Selective loss of these high-threshold fibers would explain how ABR thresholds can recover despite such significant noise-induced neuropathy. A selective loss of high-threshold fibers may contribute to the problems of hearing in noisy environments that characterize the aging auditory system.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms.

              Common causes of hearing loss in humans - exposure to loud noise or ototoxic drugs and aging - often damage sensory hair cells, reflected as elevated thresholds on the clinical audiogram. Recent studies in animal models suggest, however, that well before this overt hearing loss can be seen, a more insidious, but likely more common, process is taking place that permanently interrupts synaptic communication between sensory inner hair cells and subsets of cochlear nerve fibers. The silencing of affected neurons alters auditory information processing, whether accompanied by threshold elevations or not, and is a likely contributor to a variety of perceptual abnormalities, including speech-in-noise difficulties, tinnitus and hyperacusis. Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional 'hearing loss' arising from several common causes in humans.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Syst Neurosci
                Front Syst Neurosci
                Front. Syst. Neurosci.
                Frontiers in Systems Neuroscience
                Frontiers Media S.A.
                1662-5137
                12 May 2020
                2020
                : 14
                : 25
                Affiliations
                [1] 1Department of Otolaryngology-Head and Neck Surgery, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital , Shanghai, China
                [2] 2Otolaryngology Institute of Shanghai Jiao Tong University , Shanghai, China
                [3] 3Shanghai Key Laboratory of Sleep Disordered Breathing , Shanghai, China
                [4] 4School of Communication Sciences and Disorders, Faculty of Health, Dalhousie University , Halifax, NS, Canada
                Author notes

                Edited by: Preston E. Garraghty, Indiana University Bloomington, United States

                Reviewed by: Todd M. Mowery, New York University, United States; Jean Defourny, Fonds National de la Recherche Scientifique (FNRS), Belgium

                *Correspondence: Zhengnong Chen jassey@ 123456126.com Jian Wang Jian.Wang@ 123456dal.ca

                These authors have contributed equally to this work

                Article
                10.3389/fnsys.2020.00025
                7235317
                bc601c33-4502-400d-926f-5888dfc15170
                Copyright © 2020 Fan, Zhang, Wang, Li, Xing, Yin, Chen and Wang.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 28 January 2020
                : 16 April 2020
                Page count
                Figures: 6, Tables: 0, Equations: 1, References: 92, Pages: 11, Words: 8622
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81770998, 81800919
                Categories
                Neuroscience
                Original Research

                Neurosciences
                noise exposure,synaptic loss,coding-in-noise deficits,guinea pigs,toughening,conditioning,priming

                Comments

                Comment on this article